Lecture 2 Flashcards
1
Q
Physiology of Pain
A
- Nociceptive: produced by injury
- Neuropathic: nerve involvement
- Psychogenic: origin of psychological nature
2
Q
Opioid Analgesics
A
- Alter pain perception
- Used in moderate to severe pain
3
Q
Opioid Analgesics are indicated in?
A
- Acute pain
- Chronic Pain
- Antitussive (codeine in cough medicine)
4
Q
Endogenous opioids
A
- influence behavior (addiction)
- control pain and inflammation
- example: Endorphins
5
Q
Opioid Receptors
A
- Mu: mediating analgesia effect, most important
- Kappa: Psychotic effects
- Delta: Increase hormonal release; inhibits neurotransmitter release
6
Q
Classification of opioids
A
- Strong agonists: severe pain
- Moderate agonists: moderate pain, antitussive
- Mixed Agonists/ Antagonists: decreased risk of fatal overdose, fewer addictive qualities
- Antagonists: help with overdoses, chronic pain
7
Q
Metabolic inactivation of drugs takes place primarily in?
A
- the liver
8
Q
Opioid Mechanisms of Action can occur at which 3 different levels?
A
- Spinal Cord level
- Supraspinal Level
- Peripheral Effects
9
Q
Opioids act at the spinal cord level
A
- inhibit painful impulses being sent from the peripheral to the brain
- Bind to presynaptic nerve terminals: block synaptic transmission
- Bind to postsynaptic terminals: block neurotransmitter, Decrease excitability of postsynaptic neuron
10
Q
Opioid at Supraspinal Level
A
- identified in the brain associated with pain transmission
- exert analgesic effect by binding to supraspinal receptors
-* Activating the descending pathways
11
Q
Opioid at peripheral
A
- receptors exist outside the CNS
- peripheral ends of primary afferent (sensory) neurons
- creating analgesic effect by decreasing the excitability of sensory neurons
12
Q
Opioids: Clinical applications
A
- moderate to severe pain
- acute pain following surgery
- cancer related chronic pain
- maintain plasma concentrations
- with anesthesia
- Pulmonary edema to improve sense of ability to breathe
12
Q
Adverse effects of Opioids
A
- Sedation
- Mood changes
- Confusion
- Respiratory Depression
- Orthostatic hypotension
- Nausea / vomiting
- Constipation
- Tolerance / Dependence
13
Q
Special Concerns of Opioids for rehab patients
A
- Sedation & GI discomfort
- Timing of peak analgesic effect during rehab sessions
- Respiratory response to exercise
- Opioid-induced constipation
-Withdrawal - Methadone (helps people to get off medication without too much withdrawal)
14
Q
Opioid Induced hyperalgesia
A
- Pain may worsen when drug is taking peak effect
- Pain may improve when drug effects are minimal
- Pain may improve when dosage is reduced
15
Q
Prostaglandins (NSAIDS)
A
- trauma / disturbances in homeostasis increase prostaglandin production
- protective when it comes to responding to cellular injury
- Mediate painful effects of injury and other effects of pathology
16
Q
Prostaglandins effect
A
- Increase inflammatory response
- Increase sensitivity of pain receptors
- Fever
- Dysmenorrhea ( affect menstrual cramps)
- Thrombus formation (blood clot)
17
Q
Primary effects of NSAIDS
A
- Analgesic
- Anti-inflammatory
- Antipyretic (for fever)
- Anticoagulant
- Possibly anticancer
18
Q
Reye’s syndrome
A
- may be triggered by Asprin
- Children and teenagers
- Following the flu or chickenpox
- High Fever
- Vomiting
- Liver dysfunction
- Unresponsiveness / delirium
- Death
19
Q
COX Enzyme
A
- first step in the synthesis of prostaglandins and thromboxane
- Involved in producing pain, inflammation, fever and clotting
20
Q
What is the key site of NSAID action within the cell
A
COX
21
Q
COX 1
A
regulate normal cell activity
22
Q
COX 2
A
produced primarily in injured cells
23
Q
Best clinical effects are achieved by?
A
- inhibiting harmful prostaglandins from COX 2 while sparing production of COX 1
24
NSAIDS: mechanism of action
- inhibit synthesis of prostaglandins
- Inhibit COX 2
25
What is the potent inhibitor of COX enzymes
- Aspirin (NSAID)
26
Aspirin - clinical applications
- treatment of pain and inflammation
- treatment of fever
- treatment of vascular disorders
- Prevention of Cancer
27
what is the primary problem with all NSAIDS?
gut tissue damage
28
Susceptible patient populations of Adverse effects of aspirin like drugs
- Advanced age
- History of ulcers
- Used of multiple NSAIDs
- High doses of NSAIDs
- use of anti-inflammatory steroids or anticoagulants
29
Adverse effects of aspirin like drugs
- inhibit platelet activity
- increase blood pressure (inhibit vasoactive substances)
- less vascular tone, increased bp, chance of MI or stroke
30
COX 2 Selective Drugs
- inhibit synthesis of prostaglandins in pain and inflammation
- Spare production of beneficial prostaglandins in the stomach, kidneys and platelets
- Decrease pain and inflammation with less toxicity
31
COX 2 drugs and risk of heart attack
- COX 2 selective drugs will inhibit the production of enzymes that promote vasodilation and inhibit platelet-induced occlusion
- Clot formation can more easily occur
32
Acetaminophen
- Analgesic, fever reducer (similar to aspirin)
- NO anti-inflammatory or anticoagulant effects
- No GI tract irritation
- first line drug for pain reduction (OA)
33
Adverse effects of Acetaminophen
- No GI effects, but can cause liver issues (liver necrosis)
- can bind and inactivate liver proteins
- produce oxidative stress, mitochondrial dysfunction that triggers liver tissue destruction
34
Duloxetine (Cymbalta)
*Only FDA approved antidepressant for neuropathic pain
- SNRI
- Depression
- Anxiety
- often prescribed by pain physicians
35
